ArticleHuman molecular genetics2009
Common fragile sites are characterized by histone hypoacetylation.
Article in Human molecular genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 92 citations in OpenAlex.
- Inhibition of DEK restores hematopoietic stem cell function in Fanconi anemia.The Journal of experimental medicine · 2025Article
- Replication fork stalling in late S-phase elicits nascent strand degradation by DNA mismatch repair.Nucleic acids research · 2024Article
- Insights into common fragile site instability: DNA replication challenges at DNA repeat sequences.Emerging topics in life sciences · 2023Article
- Confined migration induces heterochromatin formation and alters chromatin accessibility.iScience · 2022Article
- Fragile sites, chromosomal lesions, tandem repeats, and disease.Frontiers in genetics · 2022Review
- Sites of chromosomal instability in the context of nuclear architecture and function.Cellular and molecular life sciences : CMLS · 2021Review
- Visualizing locus-specific sister chromatid exchange reveals differential patterns of replication stress-induced fragile site breakage.Oncogene · 2020Article
- Review
- Genome-wide mapping and profiling of γH2AX binding hotspots in response to different replication stress inducers.BMC genomics · 2019Article
- Pathways for maintenance of telomeres and common fragile sites during DNA replication stress.Open biology · 2018Review
- DNA polymerases eta and kappa exchange with the polymerase delta holoenzyme to complete common fragile site synthesis.DNA repair · 2017Article
- Rescue from replication stress during mitosis.Cell cycle (Georgetown, Tex.) · 2017Review
- WWOX: a fragile tumor suppressor.Experimental biology and medicine (Maywood, N.J.) · 2015Review
- Are common fragile sites merely structural domains or highly organized "functional" units susceptible to oncogenic stress?Cellular and molecular life sciences : CMLS · 2014Review
- Molecular characterization of common fragile sites as a strategy to discover cancer susceptibility genes.Cellular and molecular life sciences : CMLS · 2014Review
- Interplay between genetic and epigenetic factors governs common fragile site instability in cancer.Cellular and molecular life sciences : CMLS · 2014Review
- Papillomavirus genomes associate with BRD4 to replicate at fragile sites in the host genome.PLoS pathogens · 2014Article
- Causes and consequences of replication stress.Nature cell biology · 2014Review
- How unfinished business from S-phase affects mitosis and beyond.The EMBO journal · 2013Review
- Cancer as a dysregulated epigenome allowing cellular growth advantage at the expense of the host.Nature reviews. Cancer · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Common fragile sites (CFSs) represent large, highly unstable regions of the human genome. CFS sequences are sensitive to perturbation of replication; however, the molecular basis for the instability at CFSs is poorly understood. We hypothesized that a unique epigenetic pattern may underlie the unusual sensitivity of CFSs to replication interference. To examine this hypothesis, we analyzed chromatin modification patterns within the six human CFSs with the highest levels of breakage, and their surrounding non-fragile regions (NCFSs). Chromatin at most of the CFSs analyzed has significantly less histone acetylation than that of their surrounding NCFSs. Trichostatin A and/or 5-azadeoxycytidine treatment reduced chromosome breakage at CFSs. Furthermore, chromatin at the most commonly expressed CFS, the FRA3B, is more resistant to micrococcal nuclease than that of the flanking non-fragile sequences. These results demonstrate that histone hypoacetylation is a characteristic epigenetic pattern of CFSs, and chromatin within CFSs might be relatively more compact than that of the NCFSs, indicating a role for chromatin conformation in genomic instability at CFSs. Moreover, lack of histone acetylation at CFSs may contribute to the defective response to replication stress characteristic of CFSs, leading to the genetic instability characteristic of this regions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.